This subtype represents ~ 15% of CRC cases and is characterised by defective DNA mismatch repair machinery, resulting in an increased rate of mutagenesis as compared with microsatellite stable tumours (MSS).18 Furthermore, MSI CRC tumours display increased infiltration with CD8+ T cells, B cells and macrophages, as well as an increased expression of Th1-related genes.19,20. This evidence concerns the gene CD8A and colorectal carcinoma.